Seroprevalence of Various Infectious Agents in Dogs with Suspected Acute Canine Polyradiculoneuritis

Abstract

Background: Acute canine polyradiculoneuritis (ACP) is considered to be an animal model of the acute axonal form of Guillain-Barre´syndrome (GBS) in humans. Various antecedent events have been associated with GBS, including bacterial or viral infection. The relationship between ACP and previous infection requires additional attention.Hypothesis: We hypothesized a relationship between ACP and serological evidence of exposure to Ehrlichia canis, Borrelia burgdorferi, Toxoplasma gondii, Neospora caninum, Campylobacter jejuni, and canine distemper virus (CDV).Animals: Eighty-eight client-owned dogs, 44 with ACP, 44 age-matched controls.Methods: Retrospective study with stored serum samples. Serum antibodies against the target organisms were measured with commercially available assays. Sera from dogs with and without ACP that were positive for T. gondii IgG by ELISA were assayed by an IgG heavy chain-specific, Western blot immunoassay.Results: Dogs with ACP (55.8%) were more likely to have T. gondii IgG serum antibody titers than dogs without ACP (11.4%). Serum antibodies from 8 affected dogs and 11 control dogs bound to T. gondii antigens with apparent molecular masses of 67, 61, 58, 45, 33, 24, 9, and 6 kDa. An antigen with an apparent molecular mass of 36 kDa was recognized by 2 dogs with ACP but none of the control dogs.Conclusions: Results of this study suggest that ACP in some dogs, like GBS in some humans, may be triggered by T. gondii and a prospective study should be performed to further evaluate this potential association.

Anti‐GM2 ganglioside antibodies are a biomarker for acute canine polyradiculoneuritis

“…)‐infections (McGlennon et al ., ) . Recent investigations have discussed T. gondii as a possible aetiological agent for Ab‐production in ACP (Holt et al ., ) , whilst a T. gondii infection associated with GBS has also been reported (Bossi et al ., ) . In this study, only 1/14 ACP dogs assessed for a T. gondii infection was positive for T. gondii Abs and at the same time exhibited anti‐GM2 Abs.…”

Distal polyneuropathy in an adult Birman cat with toxoplasmosis

“…1 The case we reported fulfilled at least three of the above criteria. Regarding the presence of appropriate clinical signs, as no other case of polyneuropathy associated with toxoplasmosis in cats was previously described it may be difficult to support the fulfilling of this criterion; however, as reported above, toxoplasmosis is a recognised differential diagnosis of polyneuropathy in dogs, 10–12 and it has been previously discussed by other authors as a possible cause of similar signs in cats. 14 Despite the absence of direct parasite identification on histopathology, a causal relation between T gondii and the clinical signs in this case is suggested by the serology titres compatible with active infection at both initial presentation and relapse (significant increase of IgG in 4 weeks from clinical recurrence) and by the rapid response to clindamycin in three different occasions.…”

“…3 Non-suppurative myelitis/meningomyelitis and intracranial granuloma with histological identification of T gondii or Toxoplasma -like parasites have been previously documented in cats with neurological signs including seizures, circling, altered behaviour, blindness, anisocoria, ataxia, para-/hemi-/tetraparesis or paraplegia. 3–9 Considering the association between toxoplasmosis and polyradiculoneuritis in dogs, 10–12 the potential for T gondii to affect the peripheral nervous system in cats has always been suspected; however, to our knowledge, no clinical report confirming this hypothesis has been published previously. Herein we describe clinical, serological, electrodiagnostic, histological findings and treatment in an adult Birman cat presented for progressive neuromuscular signs associated with distal polyneuropathy and serologically confirmed toxoplasmosis.…”

Acute Lower Motor Neuron Tetraparesis

“…28 Another potential triggering factor recently described for dogs with AIP is Toxoplasma gondii infection. 29 In both AIP and GBS, in addition to humoral mechanisms, there is also evidence for cell-mediated immune responses involving autoreactive CD41 T cells, interferon-g, proliferating B cells, and macrophages that directly or indirectly damage myelin and axons. 2 The immune-mediated reaction in AIP seems to target ventral (motor) nerve roots and spinal nerves primarily, with variable but always minor involvement of dorsal nerve roots.…”

“…28 The demonstration of circulating serum Abs to confirm serologic exposure to different infectious agents, especially Toxoplasma gondii, is also recommended in AIP in order to detect the potential triggering factors. 29 Finally, peripheral nerve biopsy or nerve root biopsy can render information to reach a definitive diagnosis. Histologic findings include leukocytic infiltration of varying composition and intensity (more obvious in the ventral nerve roots and spinal nerves) (Fig.…”